Osteoporosis caused by type 2 diabetes mellitus (T2DM) increased the risk of fracture and post-fracture mortality. However, the pathogenesis of the disease remains unclear, resulting in a lack of effective strategies for its prevention and treatment. In this review, firstly, the effects of advanced glycation end products (AGEs) produced by non-enzymatic glycation on bone matrix composition, bone structure, and mechanical properties of T2DM were summarized. Then, the biological mechanism of AGEs and receptor for AGEs (RAGE) affecting bone degeneration in T2DM was clarified. Finally, antidiabetic and other drugs that were beneficial to bone anabolism were discussed. These drugs positively affect bone quality through inhibiting AGE/RAGE signaling pathway. Accordingly, it is expected to provide potential intervention targets and ideas for the prevention and treatment of T2DM-related osteoporosis.c